Caffeic acid phenethyl ester modulates Helicobacter pylori‐induced nuclear factor‐kappa B and activator protein‐1 expression in gastric epithelial cells

Abstract

1 Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives (honeybee resin), has anti-inflammatory, anti-carcinogenic and anti-bacterial properties. This study was designed to investigate the anti-inflammatory effects of CAPE on Helicobacter pylori-induced NF-kB and AP-1 in the gastric epithelial cell line AGS. 2 Electrophoretic mobility shift assay was used to measure NF-kB-and AP-1-DNA binding activity. Western blotting was used to detect IkB-a and COX-2 expression in AGS cells cocultured with H. pylori. The antiproliferative effect of CAPE was measured by MTT assay. 3 Our results showed that caffeic phenethyl ester inhibits H. pylori-induced NF-kB and AP-1 DNAbinding activity in a dose (0.1-25 mg ml À1 B0.35-88 mM) and time-(15-240 min) dependent manner in AGS cells. Maximum inhibition by CAPE was observed at concentrations of 25 mg ml À1 (B88 mM) CAPE prevented H. pylori-and cytokine-induced degradation of IkB-a protein.4 Pretreatment of AGS cells with CAPE also blocked cytokine-and mitogen-induced NF-kB and AP-1 expression. Furthermore, CAPE suppressed H. pylori-induced cell proliferation and production of the cytokines TNF-a and IL-8. In addition, CAPE blocked H. pylori-induced COX-2 expression. 5 The inhibition of such transcription by CAPE could result in suppression of many genes during H. pylori-induced inflammation, and also provide new insights into the anti-cancer and antiinflammatory properties of CAPE.

Catechols in caffeic acid phenethyl ester are essential for inhibition of TNF‐mediated IP‐10 expression through NF‐κB‐dependent but HO‐1‐ and p38‐independent mechanisms in mouse intestinal epithelial cells

“…1 T cells and the gastric epithelium [36,37], we could show that phosphorylation of NF-kB and IkBa, degradation of IkBa and RelA nuclear translocation were unchanged in Mode-K cells after CAPE treatment, suggesting that effects are cell/tissue type-specific. However, our results are in agreement with two previous reports which demonstrated that CAPE has no effect on IkBa degradation in osteoclasts [38] and U937 cells [7].…”

Protective effect of caffeic acid phenethyl ester against cadmium-induced renal damage in mice

“…Moreover, NF-κB activation is thought to link with oxidative stress, cytotoxic cytokines and liver cell necrosis (Liu et al, 1995). CAPE is a well-documented inhibitor of NF-κB (Abdel-Latif et al, 2005;Natarajan et al, 1996), by intervening in IKK-IκBα-p65 pathway or activating nuclear factor erythroid 2 related factor 2 (Nrf2) (Ang et al, 2009;Onori et al, 2009;Toyoda et al, 2009;Lee et al, 2010). Nrf2, an important cytoprotective transcription factor, binds to antioxidant responsive element and is a chief regulator of a battery of cytoprotective genes.…”

Quantitative determination of fluorinated caffeic acid phenethyl ester derivative from rat blood plasma by liquid chromatography-electrospray ionization tandem mass spectrometry

“…In recent years, interest in CAPE has increased not only as a potential active pharmacologic agent but also mainly as prospective raw material for pharmaceutical industry as either a starting or intermediate material for the synthesis of closely related compounds. Numerous pharmacological activities have been reported for CAPE including anticancer/tumor [2,3], antiviral [4,5], anti-inflammatory [6,7], and antioxidant [8][9][10]. Our previous studies have identified a newly synthesized CAPE derivative, FCAPE (Fig.…”